Fig. 7

IGF2BP3 can bind to and maintain the stability of circGNB1 and IGF2BP3 can mediate the promoting effects of circGNB1 on GSCs. a Identification and intersection of RBPs (IGF2BP3, FUS) potentially bound to circGNB1 based on CSCD, circInteractome, and Starbase. b, c qRT-PCR showed that IGF2BP3 knockdown or overexpression significantly affected the expression of circGNB1, whereas FUS knockdown or overexpression couldn’t. d, e The RIP assay was performed after IGF2BP3 knockdown or overexpression, followed by qRT-PCR to detect the enrichment of circGNB1. f, g The RNA pull-down assays showed IGF2BP3 protein immunoprecipitation with circGNB1 as detected by western blotting. h qRT-PCR assay was performed to detect the relative expression levels of circGNB1 treated with actinomycin D at different time points in IGF2BP3 knockdown GSC27. i–m MTS (i), Edu (j, k), and transwell (l, m) assays revealed circGNB1 knockdown could reverse the cell viabilities, proliferation capacities, and invasion abilities promoted by IGF2BP3 overexpression. n–q The neurosphere formation (n, o) and limiting dilution assays (p, q) showed circGNB1 knockdown could reverse the neurosphere formation facilitated by IGF2BP3 overexpression. Data represent mean ± SD (three independent experiments). *p < 0.05; **p < 0.01; ***p < 0.001